Lincomycin, as one of the most commonly used antibiotics, may cause intestinal injury, enteritis and other side effects, but it remains unknown whether these effects are associated with microbial changes and the effects of different doses of lincomycin on infants. Here, 21-day old mice were exposed to 1 and 5 g/L lincomycin to explore the effects of lincomycin on the gut microbiota, metabolites and inflammation. Compared to the control mice, 1 g/L lincomycin exposure decreased the body weight gain of mice (p < 0.05). Both 1 and 5 g/L lincomycin exposure reduced the diversity and microbial composition of mice (p < 0.05). Furthermore, 1 and 5 g/L lincomycin reduced the relative concentrations of acetate, propionate, butyrate, valerate, isobutyric acid and isovaleric acid in the colon chyme of mice (p < 0.05). In addition, 5 g/L lincomycin exposure reduced the villus height, crypt depth, and relative expression of TLR2, TLR3, TLR4, IL-18, TNF-α, and p65 in the jejunum of mice (p < 0.05), while 1 g/L lincomycin exposure reduced the relative expression of TLR2, TLR3, TNF-α, and p65 (p < 0.05). Collectively, these results highlight the depletion effect of short-term lincomycin exposure on microbiota and the further regulatory effect on intestinal morphology and immunosuppression in infant mice.

The adverse effects of short-term megadose of antibiotics exposure on the gastrointestinal and liver tissue reactions in young children have been reported. Antibiotic-induced intestinal and liver reactions are usually unpredictable and present a poorly understood pathogenesis. It is, therefore, necessary to develop strategies for reducing the adverse effects of antibiotics. Studies on the harm and rescue measures of antibiotics from the perspective of the gut–liver system are lacking. Here, we demonstrate that lincomycin exposure reduced body weight, disrupted the composition of gut microbiota and intestinal morphology, triggered immune-mediated injury and inflammation, caused liver dysfunction, and affected lipid metabolism. However, baicalin administration attenuated the lincomycin-induced changes. Transcriptome analysis showed that baicalin improved immunity in mice, as evidenced by the decreased levels of intestinal inflammatory cytokines and expression of genes that regulate Th1, Th2, and Th17 cell differentiation, and inhibited mucin type O-glycan biosynthesis pathways. In addition, baicalin improved liver function by upregulating the expression of genes involved in bile acid secretion and lipid degradation, and downregulating genes involved in lipid synthesis in lincomycin-treated mice. Bile acids can regulate intestinal immunity and strengthen hepatoenteric circulation. In addition, baicalin also improved anti-inflammatory bacteria abundance (Blautia and Coprobacillus) and reduced pathogenic bacteria abundance (Proteobacteria, Klebsiella, and Citrobacter) in lincomycin-treated mice. Thus, baicalin can ameliorate antibiotic-induced injury and its associated complications such as liver disease.

This study aimed to evaluate the effects of optimal carbohydrase mixture (OCM) on macronutrients and amino acid digestibility and the digestible energy (DE) in growing pigs fed the corn-soybean meal-based diet (CSM) and the wheat-soybean meal-based diet (WSM). A total of 36 ileal-cannulated pigs (50.9 ± 4.9 kg initial body weight) were allotted to four dietary treatments randomly, which included CSM and WSM diets, and two diets supplied with corresponding OCM. These OCMs were screened using an in vitro method from our previous study. After the five day adaptation period, fecal samples were collected from d six to seven, and ileal digesta samples were collected on d 8 and 10. Chromic oxide was added as an indigestible marker. The results show that the addition of OCM improved the apparent ileal digestibility (AID) of dry matter (DM), ash, carbohydrate (CHO), neutral detergent fiber, and gross energy (GE) and the apparent total tract digestibility (ATTD) of DM, CHO, and GE in CSM diet (p < 0.05), but reduced the apparent hindgut disappearance (AHD) of DM in CSM diet (p < 0.05). The ATTD of DM, crude protein (CP), ether extract (EE), ash, and GE and the AHD of DM, CP, EE, ash, CHO, and GE in WSM diet were improved by the OCM addition (p < 0.05), whereas the AID of DM, CP, ash, CHO, and GE were decreased (p < 0.05). The respective DE contents in CSM and WSM diets were increased from 15.45 to 15.74 MJ/kg and 15.03 to 15.49 MJ/kg under the effects of OCM (p < 0.05). Similar to the trend of AID of CP, the OCM addition increased the AID and standardized ileal digestibility (SID) of Ile, Thr, and Cys in CSM diet, but decreased the AID and SID of Ile, Phe, Thr, Val, Ala, Pro, Ser, and Tyr in WSM diet. In conclusion, the OCMs screened by an in vitro method could improve the total tract nutrient digestibility and DE for pigs fed corn-based diet or wheat-based diet but had inconsistent effects on the ileal digestibility of nutrients and energy.

Microplastics are ubiquitous in livestock settings and raise increasing concern, yet studies on their effects on poultry intestinal health and gut microbiota, particularly in native Chinese breeds, are still scarce. Chahua chicken No. 2 were exposed to drinking water with 0, 0.05, 0.1, or 0.5 mg/d polystyrene microplastics (PS-MPs). At 0.5 mg/d, PS-MPs significantly reduced body weight, average daily gain, and feed intake at 42 and 120 days, while increasing feed conversion ratio and decreasing carcass traits (semi-eviscerated yield, eviscerated yield, breast and thigh muscle weights) at 42 days ( p < 0.05). This dose also increased the microplastic-associated fluorescence signal in jejunum and ileum, reduced villus height and villus height/crypt depth ratio, and deepened crypts. It downregulated genes associated with intestinal barrier integrity ( ZO-1 , Occludin , Claudin-1 ), upregulated inflammatory cytokines ( IL-6 , IL-8 , IL-1β , TNF-α , MIP-1β ), and suppressed genes involved in glucose ( SLC5A1 and SLC2A2 ), lipid ( SLC27A4 , APOA1 , APOB , MTTP , CD36 , FABP2 ), and amino acid ( SLC15A1 , SLC7A1 , SLC7A9 , SLC3A1 , SLC6A19 ) transport ( p < 0.05). 16S rRNA gene sequencing analysis revealed that 0.5 mg/d PS-MPs exposure induced intestinal microbiota dysbiosis in Chahua chicken No. 2, characterized by an increased abundance of norank_o_Clostridia_UCG_014, Mediterraneibacter, Olsenella , and Faecalitalea ( p < 0.05). Overall, these findings indicate that PS-MP exposure is associated with alterations in growth performance, intestinal morphology, barrier-related gene expression, inflammatory responses, nutrient transporter expression, and gut microbiota in Chahua chicken No. 2.